摘要
目的 :观察热应激对大鼠心肌细胞线粒体氧化磷酸化和钙代谢功能的影响、研究线粒体膜渗透性转换 (PT)的变化及其病理学意义、探索热应激心肌细胞损伤发生机制。方法 :用Klark氧电极极谱法测定线粒体呼吸功能 ,用生物发光法测定心肌ATP含量及线粒体Ca2 +。ATP酶活性 ;用电感耦合等离子 原子发射光谱仪测定线粒体内Ca2 +含量 ,用分光光度法测定线粒体膜PT。结果 :热应激大鼠心肌细胞线粒体的呼吸控制率 (RCR)及氧化磷酸化效率 (P/O)均随热应激强度的增强呈显著逐步降低趋势 ;心肌线粒体Ca2 + ATP酶活性和Ca2 +含量亦明显下降 ;暴露于Ca2 +超载和氧化应激状态的线粒体 ,膜PT发生明显变化 ,钌红、抗氧化剂及反应体系酸化状态的纠正能够有效阻抑PT变化。结论 :线粒体结构与功能的破坏在热应激机体心功能损伤的发生中有着极其重要的意义。
Aim: In order to elucidate the mechanism of cardiomyocyte injury in heat stress, the changes of oxidative phosphorylation and calcium metalolism in cardiac mitochondria of heatexposed Wistar rats were observed. The changes of mitochondrial permeability transition and its pathological significance were studied as well. Methods: The respiratory function of mitochondria was measured by Klark oxgenelectrode polarography; Myocardial ATP content and activity of Ca 2+ ATPase in mitochondria were analyzed with bioluminescent method; Mitochondrial Ca 2+ content was assayed by ICP; PT was measured using spectrophotometer. Results: The respiratory control rate (RCR) and oxidative phosphorylation efficiency (P/O) were decreased gradually as rectal temperature (Tr) increased. The activity of Ca 2+ ATPase and Ca 2+ content were also reduced. Exposing to the Ca 2+ overload and oxidative stress, mitochondrial PT altered markedly. Ruthenium red and SOD could prevent the changes of mitochondrial PT. Conclusion: Destruction of mitochondrial structure and function may be of great significance in the development of impaired cardiac function in the heat stress.
出处
《中国应用生理学杂志》
CAS
CSCD
2000年第2期133-136,共4页
Chinese Journal of Applied Physiology
